Background Previous studies have shown that aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) lower colorectal cancer (CRC) risk. However, the lowest effective NSAID dose, treatment duration, and effects on survival are not defined. In a large population-based case–control study, we have explored the relationship between NSAID dose and duration, CRC risk and overall CRC-specific survival.
Methods The relationship between NSAID use and CRC risk was examined in 2279 cases and 2907 controls. Subjects completed food-frequency and lifestyle questionnaires. NSAID categories were low-dose aspirin (75 mg), non-aspirin NSAIDs (NA-NSAIDs) and any NSAID. Users were defined as taking >4 tablets/week for >1 month. ORs were calculated by logistic regression models and adjusted for potential confounding factors. Effect of NSAID use on all-cause and CRC-specific mortality was estimated using Logrank tests and Cox's hazard models.
Results In all, 354 cases (15.5%) were taking low-dose aspirin compared to 526 controls (18.1%). Low-dose aspirin use was associated with decreased CRC risk (OR 0.78 95% CI 0.65 to 0.92, p=0.004), evident after 1 year and increasing with duration of use (ptrend=0.004). NA-NSAID and any NSAID use were also inversely associated with CRC. There was no demonstrable effect of NSAIDS on all-cause (HR 1.11, p=0.22, 0.94–1.33) or CRC-specific survival (HR 1.01, p=0.93, 0.83–1.23).
Conclusion This is the first study to demonstrate a protective effect against CRC associated with the lowest dose of aspirin (75 mg per day) after only 5 years use in the general population. NSAID use prior to CRC diagnosis does not influence survival from the disease.
- Colorectal cancer
- cancer prevention
- non-steroidal anti-inflammatory drugs
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FVND & ET are joint first authors and contributed equally to this study.
Funding The work was funded by grants from Cancer Research UK C348/A3758, C348/A8896), Scottish government Chief Scientist Office (K/OPR/2/2/D333, CZB/4/94); Medical Research Council (G0000657-53203); Centre Grant from CORE as part of the Digestive Cancer Campaign (http://www.corecharity.org.uk). ET is funded by Cancer Research UK Fellowship C31250/A10107. FVND is funded by Cancer Research UK Clinician Scientist Fellowship C26031/A11378.
Competing interests None.
Ethics approval This study was conducted with the approval of the Multicentre Research Ethics Committee, UK.
Provenance and peer review Not commissioned; externally peer reviewed.
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